Background: Carbon monoxide (CO) poisoning is associated with direct cardiovascular toxicity. A prolonged QT interval has been noted in CO intoxicated patients in a few studies. The QT interval represents the time for both ventricular depolarization and repolarization, therefore roughly estimates the duration of an average ventricular action potential. A long QT interval is an arrhythmogenic condition in which there is an abnormally long delay during the electrical excitation (depolarization) and relaxation (repolarization) of the ventricles of the heart. The aim of this study was to check QTc interval prolongation in patients with acute CO poisoning and its relationship with a higher carboxyhemoglobin (COHb) level.
Materials and Methods: We study 36 patients at Changhua Show Chwan Memorial Hospital ER Department during 2004-2006 who were diagnosed with CO intoxication. Blood carboxyhemoglobin and 12-lead ECG were examined on admission. Corrected QT intervals (QTcs) were calculated by Bazett’s formula. Pearson’s correlation coefficient was employed for the statistical analysis.
Results: Our 36 CO intoxicated patients, aged 19-57years, consisted of 21 males and 15 females. There individuals had a mean carboxyhemoglobin levels of 27.6% ± 15.2%. There was a negative correlation between blood COHb level and exposure time (R=-.0.367, p<0.028). On admission, the QTc (422.0 ± 32.3ms) of the intoxicated patients was not significantly prolonged compared with normal (<440ms). A high COHb levels in acute CO intoxicated patients do not induce a longer QTc interval based on Pearson’s correlation coefficient analysis (R=0.122, p=0.48). Our patients had no ventricular arrhythmia.
Conclusion: In this study, we were unable to detect any effect of CO poisoning on the QTc. Thus it was not possible to predict a patient’s COHb level merely from the QTc and symptoms. Accordingly, even at a high COHb levels, but in absence of QTc prolongation, the arrhythmogenic risk of acute CO poisoning is low.